Replication of ICP0-Null Mutant Herpes Simplex Virus Type 1 Is Restricted by both PML and Sp100▿

Autor: Philippe Gripon, Roger D. Everett, Anne Orr, Carlos Parada, Hüseyin Sirma
Přispěvatelé: MRC Virology Unit, Institute of Virology, Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC), Université de Rennes (UR), Régulations des équilibres fonctionnels du foie normal et pathologique, Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Heinriche-Pette-Institute, the DFG, Stiftung für neurovirale Erkrankungen to H.S, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Jazyk: angličtina
Rok vydání: 2007
Předmět:
MESH: Neoplasm Proteins
viruses
Mutant
Fluorescent Antibody Technique
Gene Expression
Herpesvirus 1
Human

Viral Plaque Assay
MESH: Leukopenia
MESH: Base Sequence
Promyelocytic Leukemia Protein
Virus Replication
Autoantigens
MESH: Aged
80 and over

MESH: Autoimmune Diseases
Gene expression
MESH: Microscopy
Confocal

Nuclear protein
MESH: Fluorescent Antibody Technique
MESH: Aged
0303 health sciences
MESH: Middle Aged
MESH: Receptors
Antigen
T-Cell
alpha-beta

Microscopy
Confocal

biology
030302 biochemistry & molecular biology
Nuclear Proteins
Antigens
Nuclear

MESH: Transcription Factors
MESH: Splenomegaly
3. Good health
Ubiquitin ligase
Virus-Cell Interactions
Neoplasm Proteins
MESH: Herpesvirus 1
Human

MESH: Viral Plaque Assay
MESH: Autoantigens
[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology
Histone deacetylase activity
MESH: Leukemia
T-Cell

medicine.drug
MESH: DNA Primers
MESH: Gene Expression
MESH: Mutation
MESH: Immunophenotyping
Ubiquitin-Protein Ligases
Immunology
Microbiology
Immediate early protein
Cell Line
Immediate-Early Proteins
03 medical and health sciences
Promyelocytic leukemia protein
MESH: Receptors
Antigen
T-Cell
gamma-delta

Virology
medicine
Humans
MESH: Tumor Suppressor Proteins
MESH: Antigens
Nuclear

030304 developmental biology
DNA Primers
MESH: Humans
Base Sequence
Tumor Suppressor Proteins
MESH: Virus Replication
MESH: Clone Cells
MESH: Adult
MESH: Immediate-Early Proteins
biochemical phenomena
metabolism
and nutrition

MESH: Ubiquitin-Protein Ligases
Molecular biology
MESH: Male
MESH: Cell Line
MESH: Gene Rearrangement
gamma-Chain T-Cell Antigen Receptor

Trichostatin A
Insect Science
Mutation
biology.protein
MESH: Nuclear Proteins
MESH: Female
Transcription Factors
Zdroj: Journal of Virology
Journal of Virology, 2008, 82 (6), pp.2661-72. ⟨10.1128/JVI.02308-07⟩
Journal of Virology, American Society for Microbiology, 2008, 82 (6), pp.2661-72. ⟨10.1128/JVI.02308-07⟩
ISSN: 0022-538X
1098-5514
DOI: 10.1128/JVI.02308-07⟩
Popis: Herpes simplex virus type 1 (HSV-1) mutants that fail to express the viral immediate-early protein ICP0 have a pronounced defect in viral gene expression and plaque formation in limited-passage human fibroblasts. ICP0 is a RING finger E3 ubiquitin ligase that induces the degradation of several cellular proteins. PML, the organizer of cellular nuclear substructures known as PML nuclear bodies or ND10, is one of the most notable proteins that is targeted by ICP0. Depletion of PML from human fibroblasts increases ICP0-null mutant HSV-1 gene expression, but not to wild-type levels. In this study, we report that depletion of Sp100, another major ND10 protein, results in a similar increase in ICP0-null mutant gene expression and that simultaneous depletion of both proteins complements the mutant virus to a greater degree. Although chromatin assembly and modification undoubtedly play major roles in the regulation of HSV-1 infection, we found that inhibition of histone deacetylase activity with trichostatin A was unable to complement the defect of ICP0-null mutant HSV-1 in either normal or PML-depleted human fibroblasts. These data lend further weight to the hypothesis that ND10 play an important role in the regulation of HSV-1 gene expression.
Databáze: OpenAIRE